腹膜后淋巴结转移是早期宫颈癌最重要的预后因素，但其转移机制尚未阐明，且缺乏有效预测的分子标记物。我们研究发现，脂阀蛋白FLOT1高表达与宫颈癌淋巴结转移密切相关，沉默FLOT1表达后能抑制细胞的迁移和侵袭，进一步研究提示其机制可能与Akt/GSK-3β/Snail/E-cadherin通路调控的肿瘤转移早期关键事件-上皮细胞间质化(EMT)，有关。本项目拟在细胞模型中通过shRNA沉默、过表达、抑制剂干预等方法明确FLOT1是否通过Akt/GSK-3β/Snail/E-cadherin通路调控EMT过程从而进而促进宫颈癌的淋巴结转移，并在临床标本中加以证实。本项目将阐明FLOT1在宫颈癌中调控淋巴结转移的分子机制，为寻找有效预测早期宫颈癌淋巴结转移的分子标记物提供依据。

Retroperitoneal lymph node metastasis is the strongest prognostic factor for early-stage cervical cancer. However, thus far, the molecular mechanism underlying cervical cancer lymph node metastasis remains to be elucidated, and no sufficiently accurate model predicting lymph node metastasis has been established. We revealed that elevated expression of lipid rafts protein FLOT1 is correlated with cervical cancer lymph node metastasis and down-regulation of FLOT1 inhibited cellular motility and invasion; further investigation suggested that down-regulation of FLOT1 may inhibiteAkt/GSK-3b/Snail pathway to reverse epithelial-mesenchymal transition (EMT). The current project is aimed at verifying whether FLOT1 does regulate EMT by Akt/GSK-3β/Snail/E-cadherin pathway, through shRNA down-regulation, over-expression and inhibitor interfere in vitro, and finally warrating the hypothesis in clinical samples. Fulfillment of this project would provide evidence of mechanism of lymph node metastasis inducing by FLOT1 in cervical cancer as well as facilitate the searching of novel diagnostic biomarkers that could sufficiently accurate predict lymph node metastasis of early-stage cervical cancer.